CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

[Muffy]

Also, what are the implications of going into a sleep study on 1200mg of Neurontin? Would that allow for discovering SDB that might otherwise not surface due to PLMS disrupting sleep? But would it prevent knowing what role PLMS play? Is it accurate that Neurontin does not "fix" PLMS that are respiratory-induced?

There's no such thing as a "respiratory-induced PLM";
PLMs and respiratory events will generally occur at different cycles, so even when they are occurring simultaneously, a seasoned eye can usually isolate the effect of the individual components; and
When there are simutaneous events, it is always far more practical to treat respiratory events first, determine the extent of the PLM issue, and then decide if they need to be treated (generally, PLMs are far less disruptive to sleep that respiratory events. Except in kathy's case).

For example, here's a simultaneous respiratory event/PLM case:

viewtopic.php?f=1&t=25751&p=224585&hilit=plm%2A#p224585

In the first tracing, the PLMs are the dominant event, while in the second, the respiratory events appear to take center stage. In the second tracing, I believe a pressure increase is warranted.

Note that while the events in example 2 are labelled "obstructive hypopneas", they lack significant desaturations, so with the current respiratory rule (this was non-Medicare 2005) they should be scored "RERAs".

Muffy

[jnk]

. . . C'mon...tell us which one? . . .

Like most good quotes from lectures, I have never seen any real documentation, myself.

http://www.talkaboutsleep.com/message-b ... p?p=109509

I don't know if the following info is accurate or not, or how old it is, but I guess it represents one philosophy on scoring and PLMs:

Distinctions:

On the less severe side, leg movements may not be counted if they don't meet the 4/90 seconds rule: If there is an arousal present with an isolated leg movement, it will be a spontaneous arousal. If there is no arousal present, it can't be counted as anything.

Leg Movements and Respiratory Events: Leg movements that occur at the end of respiratory events are considered to be part of the respiratory arousal and are not counted as PLM's. Patients having respiratory events with kick-arousals AND additional leg movements, occurring in the middle of events or between events but not part of the last arousal, can be counted if they meet the 4/90 rule.

Leg Movements and Arousals: Often a leg movement occurs in conjunction with arousals. If the leg movement comes first or concurrently with the EEG change, the event will be considered a leg movement w/ arousal and considered for possible inclusion as a PLM subject to the 4/90 rule. If the EEG changes occur first, it is a plain arousal and not a PLM.

Leg Movements in REM: Isolated leg movements, twitches and fasciculations are common in REM and therefore PLM's are not scored during REM (also classic PLM's usually stop during REM.) Very frequent twitches/movements will be noted in the scoring notes.

Leg Movements during Wake: PLM's are not scored during Wake. Leg events during wake will be examined closely for periodicity and frequency, and if they are causing sleep onset arousals, in which case they will be noted in the scoring notes as possible restless legs. During periods of PLM's with some intervening wake periods, leg movements that might have been included as a PLM, but can not be since they are in wake, CAN be used to help meet the 4/90 rule for the surrounding events that do occur in sleep.

http://theorganizedcoach.com/scoringrules.htm

[SleepingUgly]

There's no such thing as a "respiratory-induced PLM"

and from the link you posted...

So the question is, are those respiratory events, and if so, what type. Obstructive or central, apnea or hypopnea, caused by PLMs or "causing" PLMs (BTW, respiratory events don't cause PLMs)....Sleep instability begets respiratory instability. I would offer to explain these differences (PLMs with and without associated respiratory disturbances) by the PLMs causing a hypereactive respiratory response, giving the event a little central flavor, and the unstable sleep state permitting some airway instability to occur.

Trying hard to understand this... Are you saying that sleep instability due to PLMS causes respiratory events?

So in terms of respiratory events causing PLMS, which you say they do not, are you saying that they may appear to be PLMS, but a seasoned eye will be able to see that these jerks (let's call them jerks) are due to respiratory events?

Would the latter type of respiratory-associated jerks be affected by Neurontin?

Thanks!

[-SWS]

If you happen to score borderline or high on this non-scientific HSP screening questionnaire then I personally suspect that your stimulus/response equation to poor sleep and EDS is probably highly multifactorial as a matter of both hypersensitivity and hyper-responsiveness.

I've seen this questionnaire cited several times on this forum. I don't know what established construct it's trying to measure, or anything else about its validity or reliability. It almost seems to be some kind of measure of sensory issues, as in sensory integration disorder.

Dr. Park holds that those with UARS have a hyperarousable nervous system, and that Dr. Guilleminault thinks that's why they tolerate CPAP as well (although I have yet to see anything Dr. Guilleminault has written along those lines). There is lots of information about people with UARS having lots of functional somatic syndromes, such as Irritable Bowel, Fybromyalgia, etc. I was under the impression that much of this resolves when the underlying SDB is treated. So IF there is a hyperarousable NS in UARS patients, I wonder if it's the chicken or the egg. In any event, other than being a very light sleeper, and a few other mild symptoms such as startling when a bird crashed into my window 3 feet from my head just now, leaving the contents of his GI track all over it, I don't think I qualify for whatever it is this scale is measuring.

SU, if you don't mind I'll put a placeholder on my own conversation and even conjecture about the above until after Muffy's, jnk's, Rebecca R's, et al's informative PLM & RERA discussion. THAT'S the kind of useful information I would focus on right now regarding your own past and future sleep studies. Excellent PLM information so far IMHO... Also hope to hear any PLM or RERA thoughts Kathy and others might have as well.

But I'll certainly relish coming back to discuss the above a bit more... Sleep study priorities and practicalities precede Prozac and Pool in River City IMO.

[Muse-Inc]

...I think a better understanding would be gained by considering the following concept: Sleep instability begets respiratory instability....

Ahh Muffy, if I'm reading this right, then my assumption that my reported 36 respiratory arousals were ultimately caused by sleep issues? I have always thought...incorrectly mayhap...that these might have been caused by my excess wt (hypoventilation tho no one's mentioned that word) or my hypops (no evidence of centrals) with desats. Sleep shifts cause respiratory changes? Or am I really confused?

I am one of those easily awakened by noise, light, movements (even too much air circulation). Although CPAP therapy has raised the threshold for awakenings from these, I still experience multiple frustrating nightime wakeups. Now that I have a card reader, I am going to start checking to see if they correspond to reported events as I've assumed since my pulse rate is also be increased. If I understand this quote, then these wakeups could be repiratory arousals rather than apneic events...right? I have absolutely no idea how I might be able to reduce these if the cause is independent of apneic events...other than losing more wt and improving how much sleep I get each night. Waking up this often makes me tired.

My AHI since last Nov is <1.9 with apneas occurring only 1/3 of these sleep sessions -- my therapy is deemed excellent at this point though I get tired easily.

[Muffy]

...I think a better understanding would be gained by considering the following concept: Sleep instability begets respiratory instability....

Ahh Muffy, if I'm reading this right, then my assumption that my reported 36 respiratory arousals were ultimately caused by sleep issues? I have always thought...incorrectly mayhap...that these might have been caused by my excess wt (hypoventilation tho no one's mentioned that word) or my hypops (no evidence of centrals) with desats. Sleep shifts cause respiratory changes? Or am I really confused?

"Sleep instability begets respiratory instability" is a 5-word Muffyism designed to describe some of the contributing factors to SDB. They are not in lieu of abnormal anatomical structures and tendency to collapse, they are in addition to.

The concept is borrowed (stolen) from the Madison group in

The ventilatory responsiveness to CO2 below eupnoea as a determinant of ventilatory stability in sleep

Muffy

[Muffy]

We also have to discuss this:

5-7% of my PLMs cause arousal, which translates to around 3 per hr. So, for now, looks like I am scheduled to be woken every 20 minutes I am asleep, irrespective of the state of my airway. Hopefully with prolonged application of the VPAP Adapt SV my neural networks will exhibit their plasticity and work out that they can tone down on PLMs.

because there are a number of misleading thoughts there. Like PLM arousals are evenly distributed (they tend to group), they cause awakening (they don't-- they're arousals) and ASV will do something about them (it can't).

Whatever happened to blizzardboy anyway?

Better get started on my taxes. Back later.

Muffy

[Muse-Inc]

...The ventilatory responsiveness to CO2 below eupnoea as a determinant of ventilatory stability in sleep

THANKS! Just started reading, good info!

[Rebecca R]

Muffy is right about Fluoxetine. It is on the Drugs to Avoid list when you have PLMD or RLS. I can’t even take a simple cold remedy or my PLMD exacerbates to torturous levels.

When there are simutaneous events, it is always far more practical to treat respiratory events first, determine the extent of the PLM issue, and then decide if they need to be treated (generally, PLMs are far less disruptive to sleep that respiratory events. Except in kathy's case).

Always far more practical EXCEPT when it is necessary to treat the PLMs first, determine the extent of the respiratory events, and then decide … (generally, for those of us whose severity of PLMD is so disruptive to our sleep that it masks the severity of our SDB).

. . . C'mon...tell us which one? . . .

Like most good quotes from lectures, I have never seen any real documentation, myself.

http://www.talkaboutsleep.com/message-b ... p?p=109509

CPAP is as dangerous as a bowl of cereal. The only way you can get hurt by one is if someone picks the damn thing off the nightstand and hits you over the head with it."
-Peter Farrell, CEO, ResMed

(quoted from the March 2005 ASAA lecture held in Washington D.C. entitled: "Catching Our Breath: Reflections on Diagnosis and Treatment of Obstructive Sleep Apnea.")

Thanks jnk. Perhaps he should have used a different simile. Have you seen what passes for cereal these days?



r

[jnk]

. . . Better get started on my taxes. Back later.

Muffy

Uncle/Aunt Muff,

Be careful how you document those capital losses.

Here's a folk-blues song by Chris Smither to enjoy while doing your taxes:

http://www.youtube.com/watch?v=jdojUeOr ... re=related

jeff

[-SWS]

Thanks jnk. Perhaps he should have used a different simile. Have you seen what passes for cereal these days?

That stuff can kill ya if it gets good and angry.

[SleepingUgly]

SU, if you don't mind I'll put a placeholder on my own conversation and even conjecture about the above until after Muffy's, jnk's, Rebecca R's, et al's informative PLM & RERA discussion. THAT'S the kind of useful information I would focus on right now regarding your own past and future sleep studies. Excellent PLM information so far IMHO... Also hope to hear any PLM or RERA thoughts Kathy and others might have as well.

Kathy and I had actually been PMing about the whole Neurontin-PLM-SDB issue before I tried to hijack this thread. I'm not sure if Muffy also put a placeholder on my questions, or if he's just busy calculating his federal refund... Hopefully he'll let me know whether I understood what he said or not.

(And why do I have so much trouble understanding you people? I used to be reasonably intelligent a couple of decades ago...)

[kteague]

Hey, just reading here. I have no clue about PLMD and RERA's. All I know is that the fragility of my sleep is linked to the activity of my limb movements. When they are poorly controlled, my sense of touch is hypersensitive, and things that normally I don't even notice I find downright maddening. For instance, my headgear isn't comfortable, or my t-shirt sleeve is scrunched up and I have to pull it down, or can't tolerate my chin strap. How that hypersensitivity may translate into respiratory issues is over my head.

It is good to read the criteria for defining leg movements in a sleep study, and to know it really is well defined and should at least be consistent across the board. How much of what is reported is debatable or dependent on the skill of the scorer? And why is my gut feeling that the established criteria is just the best they could settle on, not the end-all in accuracy? I know I've got a lot of gall even thinking that out loud - am I just jaded?

[Muffy]

I'm not sure if Muffy also put a placeholder on my questions...

Sort of.

Muffy just gets a little nervous when she thinks she sees another setup coming.

...or if he's...

SHE!!!

This is why people are confused.

Are you saying that sleep instability due to PLMS causes respiratory events?

No.

I'm saying

Sleep instability begets respiratory instability.

Trying to take that one step further results in a syllogism.

So in terms of respiratory events causing PLMS, which you say they do not, are you saying that they may appear to be PLMS, but a seasoned eye will be able to see that these jerks (let's call them jerks) are due to respiratory events?

Yes.

And they would more appropriately be called "Leg Movements with Associated Respiratory Events".

Would the latter type of respiratory-associated jerks be affected by Neurontin?

Probably.

Muffy

[blizzardboy]

Wow, you people have been busy. I am still here, just haven't had a chance to post.

So I have some more to tell. During my last four week trial period (which ended last Saturday), I actually trialled an Adapt SV, a Respironics BiPAP ASV and an S9 Auto. Furthermore, I am now using a loan Resmed S8 II auto until my new Adapt SV arrives later this week.

Some observations:

1. The S8 II auto gives me chronic aerophagia, much like the S8 auto did during my first trial. I presume this is because the machine is pumping me up to an inappropriate pressure during my central events as it treats all apneas the same i.e. with increased pressure. This is well backed up by the fact that the S9 gave me little aerophagia, probably no surprise given that it senses centrals and then doesn't ramp up pressure on detection.

2. The S9 confirmed the PSG results in that my centrals occur toward the end of my sleep cycle. After 6 hours of sleep I could wake up and see that my central index might be 3 per hour, or thereabouts. On falling back to sleep for another 3 hours I would wake to find that my central index had increased to 6 per hour, say. Hence, I had CI=3/hr for the first 6 hours and then CI=12/hr for the last 3 hrs.

3. By comparison of the S9 results with my blood pressure monitor I can see that my centrals correspond to the lows in my blood pressure.

4. During a camping trip with my family my central index went way down. My sleep was fairly broken due to kids having gastro, being kicked by kids, relatively uncomfortable rest, etc. So my centrals probably only occur when I reach the deeper stages of sleep.

5. I find the Adapt SV much easier to sleep with than the BiPAP ASV. The BiPAP waveform seems to be less in sync swith my natural breathing rhythm.

6. The sleep shop said that I was the most compliant person they had seen. I slept for 13 hours on my first night on the Adapt SV and have been averaging 9.5 hrs/night usage ever since.

7. I have developed acute joint pain recently. Quite odd really as each joint in my body seems to be taking its turn. The pain in any joint lasts for no more than two days, during which time it is excruciating to move, and then passes. I have had no joint repeat its pain. Neck. Sholders. Wrists. Knees. Groin. Ankles. Knuckles. Ankles. Fingers. Toes. Feet knuckles. Nearly all gone now. Possibly related to changes in my blood pH?

8. I am far less irritable when on CPAP.

9. I want to get a full cardio check. I want to get a neurologist. Quite an interesting problem to solve.

10. I also suffer from hearing and touch sensitivity.

11. Late last year I had surgery to straighten my septum and reduce my turbinates. I have noticed in the last couple of weeks that my nasal airway is finally starting to feel clearer. Both PSGs indicated that I had reduced nasal airflow.

I can't wait till the my Adapt SV arrives!